EXPRESSION OF MONOCYTE CHEMOATTRACTANT PROTEIN-1 MESSENGER-RNA IN HUMAN IDIOPATHIC PULMONARY FIBROSIS

被引:244
作者
ANTONIADES, HN
NEVILLEGOLDEN, J
GALANOPOULOS, T
KRADIN, RL
VALENTE, AJ
GRAVES, DT
机构
[1] HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115
[2] HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115
[3] MASSACHUSETTS GEN HOSP,PULM IMMUNOL & MOLEC BIOL LAB,BOSTON,MA 02114
[4] UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284
[5] BOSTON UNIV,MED CTR,DEPT ORAL BIOL,BOSTON,MA 02118
关键词
INFLAMMATION; MACROPHAGE; MONOCYTE CHEMOTAXIS;
D O I
10.1073/pnas.89.12.5371
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Macrophages are thought to play an important role in the pathologic changes associated with idiopathic pulmonary fibrosis (IPF). The mechanisms for increased monocyte/macrophage recruitment in IPF are unknown. Monocyte chemoattractant protein 1 (MCP-1) is the predominant monocyte chemoattractant secreted by a variety of different cell types in culture. We examined the expression of MCP-1 mRNA and its protein product in vivo in IPF and non-IPF lung specimens by in situ hybridization and immunocytochemistry. The cell types expressing MCP-1 in vivo were identified by immunostaining with specific antibodies. We demonstrated the expression of MCP-1 mRNA in pulmonary epithelial cells, in monocytes/macrophages, and in vascular endothelial and smooth muscle cells. Lung epithelial cells in patients with IPF strongly expressed MCP-1 mRNA and its protein product. In contrast, epithelial cells in non-IPF specimens did not express MCP-1 mRNA. Macrophages and vascular endothelial and smooth muscle cells were shown to express MCP-1 in both IPF and non-IPF lung specimens. These findings provide a basis for the understanding of the in vivo physiologic processes that mediate monocyte/macrophage recruitment and infiltration in the lung interstitium and the pathologic state contributing to an increased alveolar monocyte/macrophage population and inflammation in IPF.
引用
收藏
页码:5371 / 5375
页数:5
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